The skin and hypercoagulable states.

Hypercoagulable states (HS) are inherited or acquired conditions that predispose an individual to venous and/or arterial thrombosis. The dermatologist can play a vital role in diagnosing a patient's HS by recognizing the associated cutaneous manifestations, such as purpura, purpura fulminans, livedo reticularis, livedo vasculopathy (atrophie blanche), anetoderma, chronic venous ulcers, and superficial venous thrombosis. The cutaneous manifestations of HS are generally nonspecific, but identification of an abnormal finding can warrant a further workup for an underlying thrombophilic disorder. This review will focus on the basic science of hemostasis, the evaluation of HS, the skin manifestations associated with hypercoagulability, and the use of antiplatelet and anticoagulant therapy in dermatology.

Pilot study of the effect of ultraviolet light on pain and mood in fibromyalgia syndrome.

BACKGROUND: There is a lack of effective systemic or adequate symptomatic treatment for pain associated with fibromyalgia syndrome (FMS). Anecdotes suggest ultraviolet (UV) light may be of some benefit. PURPOSE: The purpose of the present study was to determine if UV is effective in ameliorating chronic pain in persons with FMS. METHODS: Nineteen subjects with FMS were enrolled in a controlled trial of UV and non-UV (control) tanning beds for 2 weeks, followed by randomization to receive UV or non-UV (control) exposure for 6 additional weeks. A follow-up interview was conducted 4 weeks after the last treatment. Pain was assessed with an 11-point numerical pain rating (Likert scale), a visual analogue pain scale (VAS), and the McGill Pain Questionnaire. Mood variables were also assessed. RESULTS: During the initial 2 weeks when subjects received both UV and non-UV (control) exposures, the 11-point Likert scale pain score decreased 0.44 points after exposure to UV from pre-exposure levels (S.E. = .095). Additionally, UV exposure resulted in greater positive affect, well-being, relaxation, and reduced pain levels when compared to non-UV (control) exposure (Odds Ratio [OR] = 2.80, p = 0.0059). Following the randomized treatment period, there was slight improvement in pain as measured by the McGill Pain Questionnaire in the UV group compared to the non-UV (control) group (12.2 versus 14.1; p = 0.049); the other pain scales yielded nonsignificant results. Assessment 4 weeks after the last treatment showed no significant differences in scores in the adjusted means for outcomes. CONCLUSIONS: Results from this pilot study suggest that tanning beds may have some potential in reducing pain in persons with FMS.

Reduced migration, altered matrix and enhanced TGFbeta1 signaling are signatures of mouse keratinocytes lacking Sdc1.

We have reported previously that syndecan-1 (Sdc1)-null mice show delayed re-epithelialization after skin and corneal wounding. Here, we show that primary keratinocytes obtained from Sdc1-null mice and grown for 3-5 days in culture are more proliferative, more adherent and migrate more slowly than wt keratinocytes. However, the migration rates of Sdc1-null keratinocytes can be restored to wild-type levels by replating Sdc1-null keratinocytes onto tissue culture plates coated with fibronectin and collagen I, laminin (LN)-332 or onto the matrices produced by wild-type cells. Migration rates can also be restored by treating Sdc1-null keratinocytes with antibodies that block alpha6 or alphav integrin function, or with TGFbeta1. Antagonizing either beta1 integrin function using a function-blocking antibody or TGFbeta1 using a neutralizing antibody reduced wild-type keratinocyte migration more than Sdc1-null keratinocyte migration. Cultures of Sdc1-null keratinocytes accumulated less collagen than wild-type cultures but their matrices contained the same amount of LN-332. The Sdc1-null keratinocytes expressed similar total amounts of eight different integrin subunits but showed increased surface expression of alphavbeta6, alphavbeta8, and alpha6beta4 integrins compared with wild-type keratinocytes. Whereas wild-type keratinocytes increased their surface expression of alpha2beta1, alphavbeta6, alphavbeta8, and alpha6beta4 after treatment with TGFbeta1, Sdc1-null keratinocytes did not. Additional data from a dual-reporter assay and quantification of phosphorylated Smad2 show that TGFbeta1 signaling is constitutively elevated in Sdc1-null keratinocytes. Thus, our results identify TGFbeta1 signaling and Sdc1 expression as important factors regulating integrin surface expression, activity and migration in keratinocyte and provide new insight into the functions regulated by Sdc1.